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Arteriogenesis, Angiogenesis and Vascular Remodeling 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 October 2024 | Viewed by 1213

Special Issue Editors


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Guest Editor
1. Department of Surgery, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands
2. Einthoven Laboratory for Experimental Vascular Medicine Leiden University Medical Center, 2333 ZA Leiden, The Netherlands
Interests: experimental vascular medicine; blood vessel; arteriogenesis
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Special Issue Information

Dear Colleagues,

Arteriogenesis, also frequently called collateral formation or even therapeutic angiogenesis, comprises those processes that lead to the formation and growth of collateral blood vessels that can act as natural bypasses to restore blood flow to distal tissues in occluded arteries. Both in coronary occlusive artery diseases as well as in peripheral occlusive arterial disease, arteriogenesis may play an important role in the restoration of blood flow.

Blood flow restoration in arteries affected by atherosclerosis can also be achieved through balloon angioplasty, with or without stenting, or bypass surgery. Unfortunately, these interventions may also lead to the induction of vascular remodeling, leading to intimal hyperplasia and the re-occlusion of treated vessels. In these inflammatory-driven vascular remodeling processes, many cell types, both vascular cells and immune cells, many cytokines and growth factors, as well as various noncoding RNAs or progenitor cells, may be involved. Consequently, many questions regarding the exact molecular mechanisms involved in the regulation of the vascular remodeling response in arteriogenesis and angiogenesis still need to be answered, and these answers will contribute to defining new therapeutic options.

Despite the substantial clinical potential of and many promising clinical trials on arteriogenesis and therapeutic angiogenesis, the exact molecular mechanisms involved in the multifactorial processes of vascular remodeling related to arteriogenesis and angiogenesis are still not completely understood.

This Special Issue of the International Journal of Molecular Sciences is devoted to all of the molecular aspects of arteriogenesis and collateral formation. It will contain articles that collectively provide balanced, state-of-the-art views on various aspects of arteriogenesis and the underlying regulation of vascular remodeling. We sincerely encourage you to read the papers published in Volume I (https://www.mdpi.com/journal/ijms/special_issues/Angiogenesis_Remodeling) and welcome your contributions to Volume II. We seek submissions of high-quality articles on all aspects of arteriogenesis, including, but not limited to, regulatory mechanisms, the cell types involved, state-of-the-art models, and therapeutic options. Potential topics include, but are not limited to, the following:

  • Genetic and environmental mechanisms controlling the formation and maintenance of native collateral circulation.
  • Mechanisms controlling pathophysiological formation and the maintenance of the angiogenic blood vessels.
  • Mechanisms controlling pathophysiological vascular remodeling.
  • Arteriogenesis, therapeutic angiogenesis, and peripheral arterial disease.
  • The formation of collateral arterial networks: insights from the developing embryo.
  • Multiple pathways converge in the development of collateral circulation.
  • Arteriogenesis and collateral formation.
  • Cell and gene therapy in peripheral arterial disease.
  • Epigenetic and epitranscriptomic mechanisms in arteriogenesis, angiogenesis, and vascular remodeling.
  • Non-coding RNA in vascular remodeling during arteriogenesis and angiogenesis.
  • Bone-marrow-derived cells in arteriogenesis and therapeutic angiogenesis.
  • Local and sustained drug delivery in arteriogenesis.
  • Mechanisms controlling arteriogenesis, angiogenesis, and vascular remodeling.

Prof. Dr. Paul Quax
Prof. Dr. Elisabeth Deindl
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • arteriogenesis
  • angiogenesis
  • collateral formation
  • peripheral arterial disease
  • vascular remodeling
  • atherosclerosis
  • restenosis
  • intimal hyperplasia
  • vein grafting
  • cardiovascular diseases
  • cell and gene therapy
  • critical limb ischemia
  • therapeutic angiogenesis
  • collateral circulation
  • drug delivery

Published Papers (1 paper)

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Research

16 pages, 4318 KiB  
Article
TRIM2 Selectively Regulates Inflammation-Driven Pathological Angiogenesis without Affecting Physiological Hypoxia-Mediated Angiogenesis
by Nathan K. P. Wong, Emma L. Solly, Richard Le, Victoria A. Nankivell, Jocelyne Mulangala, Peter J. Psaltis, Stephen J. Nicholls, Martin K. C. Ng, Christina A. Bursill and Joanne T. M. Tan
Int. J. Mol. Sci. 2024, 25(6), 3343; https://doi.org/10.3390/ijms25063343 - 15 Mar 2024
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Abstract
Angiogenesis is a critical physiological response to ischemia but becomes pathological when dysregulated and driven excessively by inflammation. We recently identified a novel angiogenic role for tripartite-motif-containing protein 2 (TRIM2) whereby lentiviral shRNA-mediated TRIM2 knockdown impaired endothelial angiogenic functions in vitro. This study [...] Read more.
Angiogenesis is a critical physiological response to ischemia but becomes pathological when dysregulated and driven excessively by inflammation. We recently identified a novel angiogenic role for tripartite-motif-containing protein 2 (TRIM2) whereby lentiviral shRNA-mediated TRIM2 knockdown impaired endothelial angiogenic functions in vitro. This study sought to determine whether these effects could be translated in vivo and to determine the molecular mechanisms involved. CRISPR/Cas9-generated Trim2−/− mice that underwent a periarterial collar model of inflammation-induced angiogenesis exhibited significantly less adventitial macrophage infiltration relative to wildtype (WT) littermates, concomitant with decreased mRNA expression of macrophage marker Cd68 and reduced adventitial proliferating neovessels. Mechanistically, TRIM2 knockdown in endothelial cells in vitro attenuated inflammation-driven induction of critical angiogenic mediators, including nuclear HIF-1α, and curbed the phosphorylation of downstream effector eNOS. Conversely, in a hindlimb ischemia model of hypoxia-mediated angiogenesis, there were no differences in blood flow reperfusion to the ischemic hindlimbs of Trim2−/− and WT mice despite a decrease in proliferating neovessels and arterioles. TRIM2 knockdown in vitro attenuated hypoxia-driven induction of nuclear HIF-1α but had no further downstream effects on other angiogenic proteins. Our study has implications for understanding the role of TRIM2 in the regulation of angiogenesis in both pathophysiological contexts. Full article
(This article belongs to the Special Issue Arteriogenesis, Angiogenesis and Vascular Remodeling 2.0)
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